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Patients impacted by the Elecare Jr formulation change

Hey, MastAttackers,

I don’t want to share any details yet but I’m having a meeting next week that should hopefully move things forward with the Elecare situation.

If you have been affected by this situation, please email MastAttack with a brief description of your situation and your contact information if you would like to be contacted by the people addressing the issue.

Please use the subject line “Elecare Jr impact” so it’s easy for me to find. Use the address “[email protected].”

Thanks!
Lisa

The MastAttack 107: The Layperson’s Guide to Understanding Mast Cell Diseases, Part 67

81. Is it true almost 20% of the population might have mast cell disease?

  • We need large scale studies in order to know for sure but this is very unlikely.
  • This figure first appeared in a paper published in 2013. This study asked mast cell patients, their relatives, and healthy control subjects to complete a questionnaire about whether or not they had symptoms of mast cell disease. 17% of the patients who were in the healthy control group reported symptoms that mast cell patients may experience. However, as we all know, you can have symptoms for a lot of reasons. Just sharing symptoms doesn’t mean anything. Also, surveys and questionnaires are known to be a bad way to collect hard data. By nature, they ask leading questions and are extremely subjective.
  • This same paper also tested for CKIT mutations in 20 mast cell patients and 20 healthy controls. The mast cell patient group included patients with MCAS, systemic mastocytosis, and cutaneous mastocytosis. The paper reported that 13/20 (65%) mast cell patients had mutations in the CKIT gene while 3/20 healthy controls (15%) had mutations in the CKIT gene. However, these mutations are not known to cause mast cell disease, or any diseases, for that matter. 20 people is a TINY number for a genetics study. You need a much larger group to really know whether or not a mutation occurs in healthy people or just people with a specific disease. We are talking hundreds to thousands of people needed in order to really know.
  • Many mastocytosis patients have a specific mutation called the CKIT D816V mutation. This mutation in mast cells only occurs when the patient has a clonal mast cell disorder like mastocytosis. People in the general population do not have the CKIT D816V without having mast cell disease.
  • Currently, the only CKIT mutations known to be associated with mast cell disease are the mutations at codon 816 of the CKIT gene. The D816V mutation is overwhelmingly the most common, but there are others that same exact spot, including D816Y, and a few others. Other mutations in the CKIT mutation are not known to be associated with mast cell disease.
  • Genes mostly tell your cells how to make proteins. The reason mutations can cause diseases is because they can change the structure of the protein that is made, affecting how it works. But not all mutations cause disease. Many mutations don’t change the proteins made by genes. This means that just having a mutation does not necessarily mean you have a disease. Mutations have to be linked to a disease by experimental work showing that people with a particular mutation have a particular disease.
  • Mutations are really very common. They occur so frequently that your cells have lots of failsafes in place specifically to work around or fix mutations. There are several ways they can do this but I’m just going to talk about one right now.
  • As I mentioned above, genes tell your cells how to make proteins. Genes are made of DNA. DNA is made of tiny building blocks called nucleotides. There are four kinds of DNA building blocks. These building blocks are grouped in bundles of three. Every one of those three DNA building block bundles tells the cell how to make a little piece of the protein. Those bundles are called codons. Then the three DNA building blocks next to that bundle tell the cell how to make another little piece of the protein, and so on. Those little pieces stick together and make the full sized protein.
  • The cell is able to make a protein by reading through this gene three pieces at a time. This is how our cells use genes to make proteins.
  • So now we know that those three DNA building blocks work together to me a tiny piece of protein. There are four kinds of DNA building blocks. What piece of protein is made is determined by which three building blocks are grouped together. There are many combinations of building blocks.
  • If one of those building blocks is mutated, it could cause the wrong protein piece to be made. So it seems that each of the three building blocks is really important to making the right protein. However, this is not the case. In fact, of those three building blocks, the last one is mostly irrelevant. If it’s mutated, it will usually still make the right protein piece. In some cases, the second one isn’t important either. The first one is the most important, but having a mutation there doesn’t always mean the protein is made wrong either.
  • So genes could potentially have up to 1/3 of its building blocks mutated without causing a problem. (I’m being very general here.) This phenomenon, in which the third DNA building block in a group can be wrong without messing up the protein is called wobble. Wobble is a built in mechanism that allows cells to make mutations sometimes without consequences.
  • That’s a lot of mutations that don’t cause problems. That’s a lot of mutations that still allow the cell to make the right protein. That’s a lot of mutations without causing symptoms or disease.
  • Your genes can withstand a lot of changes to single building blocks. When a single nucleotide is changed, it is called a single nucleotide polymorphism (snp). Most of these snps don’t cause trouble at all. The only way to know which ones cause problems is to gather up a bunch of people with these mutations and study them to see if they have diseases and, if so, which ones. So just having a mutation is not enough to know if it causes diseases without further study.

For additional reading, please visit the following posts:
Gene expression and the CKIT D816V mutation
The MastAttack 107: The Layperson’s Guide to Understanding Mast Cell Diseases, Part 2
The difference between C117+ and CKIT+
Heritable mutations in mastocytosis

The MastAttack 107: The Layperson’s Guide to Understanding Mast Cell Diseases, Part 66

80. When is chemotherapy necessary for mast cell disease?

  • For mastocytosis patients, chemotherapy is used for patients with systemic mastocytosis in whom the disease is malignant (aggressive systemic mastocytosis or mast cell leukemia) or seems to be progressing towards a cancerous form of the disease (smoldering systemic mastocytosis). There are very clear cut guidelines for this. Interferon and chemotherapy are used when a patient has smoldering mastocytosis with increasing mast cell counts; aggressive systemic mastocytosis; or mast cell leukemia, in order to kill off mast cells to slow disease progression and extend a patient’s lifespan.
  • A patient who already meets the criteria for systemic mastocytosis, who has two or more B findings, is considered to have smoldering systemic mastocytosis. SSM is a transition state between indolent SM, which has a normal lifespan, and malignant forms of mast cell disease, including ASM and MCL.
  • Having two or more of the following gets you a diagnosis of SSM: mast cell aggregates that take up 30% or more of cells in a bone marrow biopsy, and/or serum tryptase over 200 ng/mL; bone marrow with too many cells in it overall, without evidence of MDS or a myeloproliferative neoplastic disease; or organ swelling that has not yet affected organ function (swelling of the liver without ascites, spleen swelling enough that it can felt by palpation, lymph nodes swollen to 2 cm or larger).
  • Patients with SSM are watched to see if their body is making lots of mast cells quickly, or if their organs are feeling the strain of too many mast cells. One of the way they check this is to see how quickly their tryptase level increases. If their provider feels that their disease is progressing, they receive chemo or interferon to try and knock the disease down enough that they don’t reach the criteria for ASM.
  • Patients are diagnosed with ASM if they meet the criteria for SM and any of the following criteria: the body not making enough blood cells, cytopenia (absolute neutrophil count below 1000/ul, hemoglobin below 10g/dl, or platelets below 100000/ul); swelling of the liver along with free fluid in the abdomen (ascites), elevated liver enzymes, or portal hypertension; swelling of the spleen along with decreased blood cells due to damage in the spleen, excessive production of blood cells by the bone marrow to compensate, and likely resolution if the spleen is removed; malabsorption in the GI tract causing low protein in the blood (albumin) and weight loss; and severe bone dysfunction, causing a series of bone breaks and large osteolytic lesions from mastocytosis.
  • ASM patients are put on chemotherapy or interferon, usually continuously, unless there is evidence that they have killed off enough mast cells to have a less dangerous disease category.
  • Mast cell leukemia patients are on chemotherapy continuously.
  • There is no described use for chemo in cutaneous mastocytosis.
  • There are situations where patients with other disease categories (ISM, MMAS, MCAS) are put on chemo drugs to try and manage symptoms or shock episodes after all other therapies have failed. While this has been mentioned in literature, there have been no studies on it.
  • Chemo drugs should be used as a last resort. They can have significant side effects and complications that cannot always be remedied by stopping the treatment.
  • Please note that while newer, targeted chemos have become more common, they are in fact chemotherapy and carry significant risks despite being more tailored, including the potential for organ damage or failure.

For additional reading, please visit the following posts:

The Provider Primer Series: Diagnosis and natural history of systemic mastocytosis (ISM, SSM, ASM)

The Provider Primer Series: Natural history of SM-AHD, MCL, MCS 

The Provider Primer Series: Mast cell activation syndrome (MCAS)

Past present

My grandmother was murdered when my father was a teenager. He spent the next several years bouncing from home to home, often staying with his friends. One of those friends became like a brother to him. Our families were very close. And when I growing up, my very best friend was that man’s daughter.

She is a year older than me and was a grade ahead in school. We lived within a mile of each other for our whole lives until she was in high school. We were together constantly, easily six or seven days a week. We had almost the same life. It is impossible to overstate how important she was to me. I loved her and wanted to be just like her.

She has struggled with addiction for more than half our lives now. Our paths diverged in high school and never crossed again. I have seen her a few times at family functions. She never looks like herself. I often see things that remind me of her or that she would like and wish I could text her to tell her. We have very different lives now. But I still miss the person she was.

I visited her today in the hospital. I had appointments in the same hospital where she is a patient. Seeing her today was a jarring experience. I wasn’t really sure what to expect. When I opened the door, she turned toward me. It was the first time in twenty years that she looked like herself. I wondered for the first time if we could ever be close again.

I stayed for a while and caught up with her before going to my appointment. My doctor and I compared my symptoms and talked about how generally improved I am. I enjoyed pretty decent health from June 2015-August 2016. “Your symptoms are more like they were after your surgery,” he commented, referring to my recovery post GI surgery in 2015. He’s right. They are.

I often wonder if the reason why I so often reach into my past to compare the present to is because I am expected to literally do this at every appointment. I’m always looking for changes since the last time I was seen. Or since the last time I felt pretty good. Or since I was diagnosed with mast cell disease. Sickness is assessed by the changes it brings about in your body, and you can only do this by dragging the past into the present.

The past can be the precarious face for the present to balance on. We can never go back. Any of us, for anything, for any reason. It is over. But sometimes it feels like I catch the past in my present. In the drudging of old wounds and deeds, pieces of our old selves and our old lives are conveyed to the now. We can fit these pieces in our growing lives. We can remake lost connections.

Our lives will never spin as freely with these old pieces, weighed down with history. But they can still be strong enough to hold you up.

The MastAttack 107: The Layperson’s Guide to Understanding Mast Cell Diseases, Part 65

79. Do probiotics help GI symptoms from mast cell disease?

  • Some people may not be aware of this, but my first science love was microbiology. I love bacteria. They are my teeny little super guys. Mostly because they make the world go round. <3
  • Yes, probiotics help symptoms from mast cell disease.
  • Your body is populated with millions and millions of microbes in just about every place where your body comes into contact with the outside world. This is mostly skin, GI tract, GU tract, and upper respiratory tract.
  • This is an example of symbiosis: the science term for “everybody wins.” Microbes get a steady source of food and protection from the outside world by living attached to some part of us. In return, they help us to break down molecules, make vitamins for us, and help protect us from infections by taking up all the available microbe real estate. If there’s already friendly bacteria (or yeast) living in every available place where microbes could attach to us, that helps to protect us from not so friendly microbes who need a place to latch on.
  • Antibiotics and antimicrobials are in tons of over the counter of products. We are in an age where antibiotics and antimycotics are being used more than ever, often in situations where they can’t even provide benefit.
  • These have the effect of killing off all the helpful microbes, leaving us in a situation where the ones that are left are the most resistant to treatment. This is a huge problem for a number of reasons, the biggest one being the genesis of super bugs, antibiotic resistant organisms that we can’t kill.
  • But there’s another big reason: when you kill off helpful bacteria, it affects our day to day bodily functions. Our bodies have evolved to have this symbiotic relationship with these organisms for millennia. When we kill all those little super guys off, our body is open to infections and situations that cause inflammation.
  • The population of microbes that normally lives happily inside our healthy bodies is called our commensal. If it’s in the GI tract, it’s called the GI commensal.
  • We know for sure that food allergies is related at least partially to changes in the GI commensal.
  • There are a number of experiments that show that if you take the GI commensal out of a healthy mouse and transplant it into a food allergic mouse, that mouse is no longer food allergic. We also know that if you take the GI commensal out of a food allergic mouse and transplant it into a healthy mouse, now you have two food allergic mice.
  • Probiotics contain microbes that you can use to replace the good ones that have been killed off. Mast cell patients, and patients with other inflammatory GI diseases, report a lot of benefit with using probiotics. Mast cell patients have to be careful and need to be sure to look up the ingredients of every probiotic they try, as many of them contain triggers, like lactose. VSL3 often works pretty well in people who are reactive. Culturelle is used by lots of patients. It depends on a lot. Your mileage may vary.
  • People with central lines should use caution and always be sure to wash hands and sterilize surfaces between taking probiotics and using their lines. These organisms are not supposed to be introduced to the bloodstream and could potentially cause infections, especially in people with depressed immunity.
  • I would to give a shout out to MastAttack admin, Pari, who is the most relentless advocate for probiotics I have ever seen. She cares more about your use of probiotics than I care about most things.

Loud

I am a dramatic person by nature. This is directly at odds with the logical habits and orderly thinking of a scientist. As you might imagine, I am not infrequently conflicted on how to behave or how to react in many situations. I am also bossy. I like to be right. These aren’t good qualities but it’s who I am and I know it.

I’m also loud in just about every way. My hair is fire engine red. I have a violet streak behind my left ear. I wear large colorful glasses. I do unusual and interesting things to my hair and trap it with flower clips or jeweled hairpieces or brightly patterned bobby pins. I dress like a 50’s housewife. I am physically loud, owing largely to my hearing loss and my inability to modulate my own voice level, but I was loud before.

It is a different loudness I’m thinking about tonight. I’m thinking about the loudness of a voice when you scream for help. This is likely the only way in which I am not loud. I used to be. It was never helpful. I am self reliant in large part because I learned early that screaming for help because I was sick or something was wrong with my body was a fruitless endeavor. It never helped and I gained a reputation as being dramatic and attention seeking, a hypochondriac. I learned to swallow those sounds, the ones that signal that I am wounded, that tell the other creatures that I am prey. This unmet need formed the core of my self esteem as a teenager, or lack thereof.

I met up with an old friend this week, a guy I went to high school with. We were friends when I was starting to become aware that something was wrong with my body. I was always having weird health issues and had episodes of inexplicable severe abdominal pain at the most inopportune times. We chatted about my health, then and now.

“So you always had this and just found out about it as an adult?” He asked.

This is more or less what happened. I’m not convinced that everything I had as a teen was related to mast cell disease, but probably a lot of it was. He mentioned that at the time, he wasn’t sure what was going on, if I was sick or just dramatic. This didn’t upset me at all, and was not new information. We have discussed this in the past, some time ago.

“I actually wasn’t sure either,” I admitted. When so many people think you are just inventing these things, it’s hard not to become convinced yourself. Still, I haven’t often said this explicitly. It seems like a betrayal of my deepest self, the one that swallows those sounds, and feels unnecessarily loud.

It has been a long time since those days, when I was 16 and confused about what exactly was happening to me and how much my mental health played a role. But even now it is a reflex to think I am being too direct. I have to remind myself that telling the world what is happening to me is okay and that wanting empathy and help is okay. I’m gaining volume. But I don’t know that I’ll ever be loud.

The MastAttack 107: The Layperson’s Guide to Understanding Mast Cell Diseases, Part 64

78. Are vaccines contraindicated for people with mast cell disease?

  • What I describe here is a summary of the current state of expert recommendations on this topic. These are not the personal opinions of Lisa Klimas.
  • Generally, vaccines are not contraindicated based solely upon having mast cell disease.
  • The big reason for this is that we know for sure that infections are mast cell activating, in addition to the array of other issues caused by having a condition serious enough to require vaccination.
  • The idea is that if you have a mast cell reaction to a vaccine, it may still grant enough protection against a specific condition, or cross coverage for related conditions, that it may be worth it. Of course, whether or not this is the case depends on a LOT of factors.
  • Vaccination will cause some level of mast cell activation in everyone, mast cell patient or otherwise. This is part of the immune response a person generates that gives them immunity from the vaccine. There is no confusion about whether or not vaccines cause mast cell activation. They do. Every time.
  • It is my experience that the patients who react worst to vaccination are patients with mast cell activation syndrome rather than those with systemic or cutaneous mastocytosis. This is my view from 10,000 feet. There are, of course, exceptions.
  • It is also my experience that the patients who react worst to vaccination often do so because they have another condition where vaccination is contraindicated, like a metabolic disorder. Additionally, I find that many of those patients also have primary immunodeficiencies, meaning they may not be able to generate a vaccine response at all, therefore making vaccination a pointless endeavor for those particular people.
  • So there are some mast cell patients who should not receive vaccines. This is not, usually, because of their mast cell disease. For most of my mast cell patienthood, I have been pretty reactive. I am fully vaccinated and continue to receive vaccines as needed.
  • Mast cell patients should be aware that the normal premedication for procedures has to be modified for vaccination. Specifically, you can’t use systemic corticosteroids for two weeks prior to vaccination in order for the vaccination to be effective. (This excludes patients taking the dose equivalent of 6 mg prednisone or less daily.) This means that antihistamines are the primary method of premedication for vaccination.
  • (Author’s note: I have gotten lots of questions about corticosteroids and vaccination. Corticosteroids are immunosuppressive so they suppress your body’s ability to generate immunity to anything, including a vaccine. If a patient receives either continuous or short burst low dose corticosteroids within two weeks before or after vaccination, most providers feel there is still benefit. However, doses above this blunt the immune response and can cause an ineffective vaccine response. As always, please speak with your provider about how this specifically applies to you. It is possible there are scenarios that this does not cover. As always, this is not medical advice.)
  • Also, I am no way diminishing or arguing that vaccines cannot cause injuries. This post is not to address that.

Introducing Mikal

We are in the process of making some changes here at MastAttack, including building a team to help manage the site, the group, and access to me, in general. We recently have begun the process of digging through the huge backlog of email and FB questions for me. This will help to prioritize things that need my attention and allow me to focus more on my health, my job and my family.

I wanted to introduce everyone to Mikal Mowdy, who has come aboard to help with MastAttack. Many of you likely remember her daughter, Yzzy, who was cured of systemic mastocytosis and hemophagocytic lymphohistiocytosis when she received a bone marrow transplant in January. She has a wealth of mast cell knowledge and will help me to respond to questions.

Please join me in welcoming Mikal!

Lisa

The MastAttack 107: The Layperson’s Guide to Understanding Mast Cell Diseases, Part 63

77. Can you have anaphylaxis with high blood pressure?

  • Yes.
  • The misconception that a person with high blood pressure cannot be experiencing anaphylaxis is enduring and dangerous.
  • Author’s note: Thanks to the intrepid reader who caught a big typo right here. When I published the post, it said, “The misconception that a person with high blood pressure can be experiencing anaphylaxis is enduring and dangerous.” This is a whopper mistake. It should say,  “The misconception that a person with high blood pressure canNOT be experiencing anaphylaxis is enduring and dangerous.” You CAN have high blood pressure and anaphylaxis at the same time. Thanks again!
  • Lots of providers (and patients) think that high blood pressure rules out anaphylaxis. This is not true.
  • This misunderstanding comes from confusing two closely related but distinct concepts: anaphylaxis and anaphylactic shock.
  • Anaphylaxis is a severe allergic reaction affecting multiple organ systems.
  • Anaphylactic shock is when anaphylaxis causes such poor blood circulation that the heart cannot pump out enough blood to the body.
  • Anaphylactic shock is a form of circulatory shock, which means exactly what I just described: oxygenated blood is not being pumped out of the heart and through the blood vessels to the tissues that need it.
  • Anaphylactic shock is defined as blood pressure 30% below the patient’s baseline or a systolic blood pressure below 90 mm Hg. The systolic blood pressure is the top number when you get your blood pressure checked. If that top number is below 90 mm Hg, and that is the result of anaphylaxis, you are in anaphylactic shock.
  • Anaphylactic shock is the most serious potential complication of anaphylaxis. Anaphylactic shock happens when the chemicals released by mast cells cause a lot of the fluid in the bloodstream to “fall out” of the bloodstream and get stuck in the tissues.
  • When this happens, that fluid loss causes the blood pressure to drop. In response, the heart beats faster to try and use the blood it still has left to get oxygen to the body. However, at a certain point, even beating really fast is not enough to get enough blood to the tissues. At this point, shock sets in.
  • Anaphylactic shock occurs specifically as a result of low blood pressure. Because of this, providers strongly associate low blood pressure with anaphylaxis. They may not realize that while a person with high blood pressure cannot be having anaphylactic shock, they can be having anaphylaxis.
  • Part of the confusion is that anaphylaxis has been defined lots of different ways by many different groups. I have written a very detailed post about this (see the link below). Even today, exactly what constitutes anaphylaxis not agreed upon by everybody.
  • The most widely used criteria in the US are the criteria published in 2006 by the World Allergy Organization journal. These criteria explicitly state that a person does not need to have low blood pressure to be having anaphylaxis. A person can meet these criteria based upon a variety of combinations of symptom and vital signs that do not include low blood pressure.
2006 WAO Anaphylaxis Criteria

For additional information, please visit the following posts:

The definition of anaphylaxis
Anaphylaxis and mast cell reactions

The MastAttack 107: The Layperson’s Guide to Understanding Mast Cell Diseases, Part 49

 

 

The MastAttack 107: The Layperson’s Guide to Understanding Mast Cell Diseases, Part 62

76. Is it true that allergic reactions can cause heart attacks?

  • Yes.
  • Kounis Syndrome is an acute coronary syndrome caused by activated mast cells releasing chemicals. It is sometimes referred to as “allergic heart attack.” In acute coronary syndrome, there is not enough blood being pumped into the heart. It is named for two of the large blood vessels supplying oxygen to the heart, the coronary arteries. When not enough blood is getting to the heart via the coronary arteries, it can damage heart muscle, sometimes permanently. Heart attack and angina are examples of acute coronary syndromes.
  • In Kounis Syndrome, mast cells become activated, releasing lots of chemicals. These chemicals can irritate the coronary artery, causing it to spasm. This spasm reduces the amount of blood getting to the heart. Sometimes, mast cell activation can trigger the formation of a clot. A clot can be the reason not enough blood is passing through the artery.
  • Several of the molecules released by mast cells can affect the cardiovascular system and contribute to causing Kounis Syndrome. Histamine and leukotrienes can cause the coronary artery to narrow. It can also activate platelets, helping a clot to form. Both tryptase and chymase can cause clots formed elsewhere to break off and get stuck in the coronary artery.
  • Mast cells also help regulate an important molecule called angiotensin II. Angiotensin II is a powerful regulator of blood pressure and can cause the coronary artery to narrow and tighten up.
  • People with Kounis Syndrome may have a history of coronary artery disease. Some patients have a stent in the coronary artery from a previous coronary issue. A stent is a tube that helps keep the blood vessel the right size so that the heart gets the blood it needs. However, many patients with Kounis Syndrome do not have any history of problems with their heart or blood vessels.
  • The symptoms of Kounis Syndrome sometimes look just like the symptoms of any other mast cell reaction or anaphylaxis, making it hard to know that a person is having Kounis Syndrome. Chest pain, irregular heart beat, the heart beating too fast or too slow, and palpitations are all common symptoms of Kounis Syndrome.
  • Another tricky thing about Kounis Syndrome is that it doesn’t always show up on the tests we use to look for heart attack or coronary issues. Because of this, doctors don’t always realize what is happening. Some people do have positive results to these tests, things like EKG, echocardiogram, chest x-ray, and bloodwork to look at levels at cardiac enzymes or troponin. Cardiac enzymes and troponins are often high in a person who is having a heart attack but are sometimes normal for patients with Kounis Syndrome.
  • In order to manage Kounis Syndrome, patients may need treatment for both the allergic reaction and the coronary syndrome.
  • Treatment for the allergic reaction is similar to anaphylaxis treatment: an H1 antihistamine like Benadryl, an H2 antihistamine like famotidine, a corticosteroid like methylprednisolone, IV fluids, and sometimes epinephrine, if that’s appropriate. Please note that epinephrine is not always appropriate for patients who have Kounis Syndrome because epinephrine can actually also cause the coronary artery to narrow.
  • Treatment for the cardiovascular aspect of Kounis Syndrome is very dependent upon symptoms and test results. Calcium channel blockers like verapamil, aspirin, and nitroglycerin are commonly used. Importantly, some of the common medications used to manage coronary syndrome are not safe for mast cell patients. These medications include beta blockers like metoprolol or atenolol, and, to a lesser extent, ACE inhibitors like lisinophil. These medications can interfere with epinephrine so epinephrine may not work if a patient needs it for anaphylaxis.
  • Anything that triggers mast cell activation can cause Kounis Syndrome, including emotional stress.

For additional information, please visit the following posts:
Kounis Syndrome: Subtypes and effects of mast cell mediators (Part 1 of 4)
Kounis Syndrome: Diagnosis (Part 2 of 4)
Kounis Syndrome: Treatment (Part 3 of 4)
Kounis Syndrome: Stress (Part 4 of 4)
Beta blockers and epinephrine
Cardiovascular manifestations of mast cell disease: Part 1 of 5
Cardiovascular manifestations of mast cell disease: Part 2 of 5
Cardiovascular manifestations of mast cell disease: Part 3 of 5
Cardiovascular manifestations of mast cell disease: Part 4 of 5
Cardiovascular manifestations of mast cell disease: Part 5 of 5
The Provider Primers Series: Medications that impact mast cell degranulation and anaphylaxis